Several special considerations of thyroid dysfunction during pregnancy should be kept in mind. First, signs and symptoms of disordered thyroid function may be mimicked by pregnancy itself. Second, increases in thyroid-binding proteins during pregnancy alter standard thyroid function tests. Third, placental transfer of most thyroid hormones is minimal. Finally, most antithyroid drugs freely cross the placenta and are potentially active in the fetal thyroid.

Profound hypothyroidism is often associated with impaired fertility and is uncommon during pregnancy. On the other hand, mild hypothyroidism is a frequent concomitant illness during pregnancy. Therapy consists of full thyroid hormone replacement. When replacement is adequate, thyroid-stimulating hormone levels return to normal, but this may take up to 8 weeks for maximum effect. There is no evidence to suggest that replacement dosages of thyroid medication suppress fetal thyroid function.

Graves’ disease is the major cause of thyrotoxicosis in women of childbearing age and thus in pregnancy. The clinical course of Graves’ disease is known to vary during gestation. Thyrotoxicosis often improves during pregnancy and worsens postpartum.

Since radioactive iodide therapy is contraindicated during pregnancy, therapeutic options include antithyroid medications and surgery. Two important points require emphasis before specific treatment of hyperthyroidism is considered. First, mild hyperthyroidism appears to be well tolerated during pregnancy. Second, antithyroid drugs freely cross the placenta and are active against the fetal thyroid.

Both propylthiouracil (PTU) and methimazole have been used successfully during pregnancy. PTU crosses the placenta only about one fourth as well as methimazole and is preferred for use during pregnancy. Propranolol has been used during pregnancy to control severe adrenergic symptoms before antithyroid medications have had sufficient time to take effect. Propranolol does not block production of thyroid hormone. Surgery should be reserved for patients with hypersensitivity to antithyroid drugs, for poorly compliant patients, and for the occasional patient in whom reasonable dosages of antithyroid drugs have been ineffective. Patients with Graves’ disease who have undergone thyroidectomy may still have high concentrations of thyroid-stimulating immunoglobulin; consequently, their offspring are vulnerable to neonatal thyrotoxicosis.